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Susan Greenfield

Publications and source records attributed to Susan Greenfield.

3 recordsLinked to original sources
PubMed2005

A peptide derived from acetylcholinesterase is a pivotal signalling molecule in neurodegeneration.

It is now widely accepted that acetylcholinesterase (AChE) also displays non-cholinergic functions, completely independent of cholinergic transmission. Indeed, AChE has been implicated in a variety of trophic and toxic actions in a range of different systems. However, it is still uncertain what part of the AChE molecule may be responsible for these actions, and indeed via what receptor. Recent work has identified a peptide towards the C-terminus of the AChE molecule that appears to have very similar effects to non-cholinergic AChE itself. This action is to enhance calcium entry, in acute and chronic preparations across a trophic-toxic spectrum, depending on concentration applied and/or duration of exposure.

Acetylcholinesterase↗
PubMed2004

Bioactivity of a peptide derived from acetylcholinesterase: involvement of an ivermectin-sensitive site on the alpha 7 nicotinic receptor.

A peptide fragment of 14 amino acids, derived from the C-terminus of acetylcholinesterase (AChE), might underlie the now well-established noncholinergic effects of the enzyme. This peptide is bioactive in a variety of systems including acute (brain slices) and chronic (organotypic culture) preparations of hippocampus, a pivotal area in Alzheimer's disease (AD); invariably, the action of the peptide is mediated specifically via an as yet unknown receptor. In this study, the allosteric alpha 7 agent, ivermectin (IVM), had a modest inhibitory effect, whilst that of the peptide was significantly more marked. However, ivermectin rendered ineffective the toxicity of high doses of the peptide, that is, when the two were co-applied, only the smaller effects of ivermectin were seen. Ivermectin, therefore, is presumably acting at a site that is identical to, or at least strongly interactive with, the normal binding site for AChE-peptide. This observation could have important implications for eventual therapeutic targeting of the action of AChE-peptide, in neurodegeneration.

Acetylcholinesterase↗